The study behind controversial research findings from the US that found a common blood test for prostate cancer has no benefit in reducing deaths has been challenged by Australias and New Zealands peak body for urological surgeons. AUCKLAND, Mar. 24 /Medianet International-AsiaNet/ --
NEW YORK, Apr 08, 2009 (ASCRIBE NEWS via COMTEX) -- A new multi-center study shows that an experimental drug lowers prostate specific antigen (PSA) levels - a marker for tumor growth - in men with advanced prostate cancer for whom traditional treatment options have failed. The study, led by researchers at Memorial Sloan-Kettering Cancer Center (MSKCC), is published today in Science Express, the online version of the journal Science
Degarelix prostate cancer drug makes testosterone levels fall dramatically and quickly3. December 2008 22:10
Researchers from Canada, the USA, France, Denmark and the Netherlands studied 610 men as part of the Phase Three trial, randomly assigning them to one of three study groups.
"Androgen deprivation hormone therapy is an effective response to prostate cancer, but the drugs that are most widely used cause an initial rise in testosterone - the hormone we are trying to reduce - when the patient first takes them" explains lead author Dr Laurence Klotz from the Division of Urology at the University of Toronto, Canada.
"We prefer to avoid this biochemical surge as it can stimulate the prostate cancer cells and exacerbate a number of clinical symptoms, such as spinal cord compression and bone pain. It could also result in more rapid growth of microscopic disease that is present in the patient but is too small to be detected.
"Degarelix is a new gonadotrophin-releasing hormone (GnRH) antagonist. It works by binding to, and blocking, the GnRH receptors in the pituitary gland, reducing the amount of LH and FSH hormones that are released. This leads directly to a rapid fall in testosterone."
Group one (207 patients) received an injection of 240mg of degarelix in month one, followed by a maintenance dose of 80mg every month for eleven months and group two (202 patients) received 240mg of degarelix in month one followed by a maintenance dose of 160mg for eleven months.
The third group (201 patients) received a monthly 7.5mg dose of leuprolide, which is a GnRH agonist.
At the start of the trial the study participants had a median testosterone level of 3.93 ng/mL. The aim was to reduce this to 0.5ng/mL or less at all monthly measurements from day 28 to day 364.
Eight out of ten study participants completed the trial (504 patients) between February 2006 and October 2007, with similar drop-out and exclusion rates in all three groups.
The key findings were impressive:
- Three days after starting their treatment regimes, 96.1 per cent of the patients on 240/80mg degarelix and 95.5 per cent of the patients on 240/160mg degarelix had achieved a testosterone level of 0.5ng/mL or less. In contrast, median testosterone levels in the leuprolide group had increased by 65 per cent by day three, but had reduced by day 28.
- At the end of the study period, 98.3 per cent of the 240/160mg degarelix group and 97.2 per cent of the 240/80mg degarelix group had achieved a testosterone level of 0.5ng/mL or less. The figure for the leuprolide group was 96.4 per cent.
- PSA levels fell much faster in the degarelix groups when measured at 14 and 28 days - by 64 per cent and 85 per cent in the degarelix 240/80mg group, 65 per cent and 83 per cent in the 240/160mg degarelix group and 18 per cent and 68 per cent in the leuprolide group.
The hormonal side-effects experienced by the three treatment groups were similar to previously reported effects for androgen deprivation hormone therapy.
Patients receiving degarelix were much more likely to experience injection-site reactions than those receiving leuprolide (40 per cent compared to one per cent).
However degarelix patients suffered fewer urinary tract infections than those in the leuprolide group (three per cent versus nine per cent) together with fewer joint pains and chills (four per cent versus nine per cent).
"More than 2,000 patients have now taken part in clinical trials for degarelix and there have been no signs of immediate or late-onset systemic allergic reactions, in contrast to other reported trials of other GnRH antagonists" points out Dr Klotz.
"The aim of the study was to show that degarelix was not inferior to leuprolide when it came to maintaining low testosterone levels over a one-year treatment period. We have conclusively shown that this is the case.
"However, we have also demonstrated that degarelix - which is an antagonist - offers an advantage, in that it reduces testosterone and PSA levels very quickly. It doesn't cause the initial surge of testosterone seen with agonist drugs like leuprolide - the other drug featured in this study.
"This is relevant as biochemical surges in testosterone can stimulate the prostate cancer cells and cause unpleasant side effects for patients. They may also require further drug therapy to counteract the effects of agonist drugs like leuprolide."
By Simeon Bennett Dec. 8 (Bloomberg) -- Drinking coffee may lower the risk of developing the deadliest form of prostate cancer, according to a Harvard Medical School study.
In research involving 50,000 men over 20 years, scientists led by Kathryn Wilson at Harvard’s Channing Laboratory found that the 5 percent of men who drank 6 or more cups a day had a 60 percent lower risk of developing the advanced form of the disease than those who didn’t consume any. The risk was about 20 percent lower for the men who drank 1 to 3 cups a day, and 25 percent lower for those consuming 4 or 5 cups.
The study is the first to associate coffee with prostate cancer, contradicting previous research that’s found no link. The difference may be because Wilson and colleagues looked for the first time at the link between coffee and different stages of the disease, instead of grouping them all together. More research is needed to confirm the findings, she said.
“People shouldn’t start changing their coffee consumption based on one study,” Wilson said in a phone interview on Dec. 5. “It could be chance, and we really need to see whether it pans out in other studies.”
Prostate cancer struck almost 200,000 men in the U.S. this year and killed more than 27,000, making it the second-deadliest malignancy among American men after lung cancer, according to the American Cancer Society. About 54 percent of U.S. adults drink coffee, according to the New York-based National Coffee Association.
The researchers aren’t sure which of the many components of coffee is responsible for the effect, though it probably isn’t caffeine because the same association was seen for decaffeinated coffee, Wilson said. The link wasn’t seen in patients with an earlier stage of prostate cancer, she said.
Coffee lowers the risk of Type 2 diabetes by increasing the body’s ability to use insulin to convert blood sugar to energy, previous research has shown.
Higher insulin levels have also been associated with an increased risk of prostate cancer, suggesting the hormone may be the link between coffee and the disease, Wilson said.
The data were presented at an American Association for Cancer Research conference in Houston.
To contact the reporter on this story: Simeon Bennett in Singapore at firstname.lastname@example.org
Last Updated: December 8, 2009 01:21 EST
ScienceDaily (Jan. 7, 2011) — Elevated fat and cholesterol levels found in a typical American-style diet play an important role in the growth and spread of breast cancer, say researchers at the Kimmel Cancer Center at Jefferson. The study, published in the January issue of The American Journal of Pathology, examines the role of fat and cholesterol in breast cancer development using a mouse model. The results show that mice fed a Western diet and predisposed to develop mammary tumors, can develop larger tumors that are faster growing and metastasize more easily, compared to animals eating a control diet.
The research team led by cancer biologist Philippe G. Frank, Ph.D., Assistant Professor in the Department of Stem Cell Biology and Regenerative Medicine at Thomas Jefferson University, was interested in learning about the link between diet and breast cancer. The incidence rate of this cancer is five times higher in Western countries than in other developed countries. Moreover, studies have shown an increase in breast cancer incidence in immigrant populations that relocate from a region with low incidence. "These facts suggest strong environmental influence on breast cancer development," says Dr. Frank.
Dietary fat and cholesterol have been shown to be important risk factors in the development and progression of a number of tumor types, but diet-based studies in humans have reached contradictory conclusions. This has led Dr. Frank to turn to animal models of human cancer to examine links between cholesterol, diet, and cancer.
The research team turned to the PyMT mouse model to determine the role of dietary fat and cholesterol in tumor development. This mouse model is believed to closely parallel the pathogenesis of human breast cancer. PyMT mice were placed on a diet that contained 21.2 percent fat and 0.2 percent cholesterol, reflective of a typical Western diet. A control group of PyMT mice was fed a normal chow that had only 4.5 percent fat and negligible amounts of cholesterol.
The researchers found that tumors began to develop quickly in mice fed the fat/cholesterol-enriched chow. In this group, the number of tumors was almost doubled, and they were 50 percent larger than those observed in mice that ate a normal diet. "The consumption of a Western diet resulted in accelerated tumor onset and increased tumor incidences, multiplicity, and burden, suggesting an important role for dietary cholesterol in tumor formation," Dr. Frank says. There was also a trend towards an increased number of lung metastasis in mice fed the fatty diet, he adds.
To confirm the aggressive nature of the cancer in animals fed a cholesterol-rich diet, the researchers examined the levels of several biomarkers of tumor progression and found a signature of a more advanced cancer stage, compared to tumors that developed in the control group.
The researchers also showed that plasma cholesterol levels in experimental mice that developed tumors were significantly reduced compared to a group of "wild-type" mice -- animals with no predisposition to develop tumors -- that was also fed a cholesterol-rich diet. "This suggests that tumor formation was responsible for the reduction in blood cholesterol levels observed in our animals," indicates Dr. Frank.
Dr. Frank explains the use of cholesterol in breast tumors this way: "In a neighborhood, if you want to build more houses, you need more bricks. In tumors, cholesterol provides the bricks that are the foundation for further growth, and this cholesterol comes from the blood. A drop in blood cholesterol may signify that some tumors are growing as cholesterol provides support for breast cancer growth."
"These data provide new evidence for an increase in cholesterol utilization by breast tumors and thus provides many new avenues for prevention, screening, and treatment," indicates Dr. Frank. These findings suggest that use of cholesterol-lowering drugs, such as statins, may both protect against breast cancer as well as treat patients carrying tumors. Since researchers also found that blood cholesterol levels dropped significantly as tumors began to develop, the study indicates measuring blood cholesterol levels may also be an effective method of screening cancer development.
This research team also discovered the same association between cholesterol and growth of prostate cancer in mice in a study published in the December issue of The American Journal of Pathology. The results of these two new studies indicate, according to Dr. Frank that, "Cholesterol does indeed seem to be an important factor in the regulation of tumor formation in several cancer types."